Previous studies showed that aversive conditioning procedures which elicited sustained hypoventilatory breathing and peripheral vasoconstriction potentiated the development of experimental hypertension in laboratory animals, but only under conditions of high sodium intake. This hypoventilatory breathing pattern has been observed to occur episodically in humans in their natural environments, to occur more frequently at work and in social situations, and to be accompanied by acute increases in blood pressure, but not heart rate. During the past year, humans have been trained to comfortably maintain hypoventilation-induced hypercapnia in the laboratory using a feedback procedure. The breathing pattern has been associated with small but sustained increases in blood pressure, decreases in heart rate, increases in pCO(2) and decreases in pH. Bicarbonate ion concentrations showed a delayed rise under these conditions. There was no evidence of increased sympathetic nervous system activity in the heart. These findings are consistent with the hypothesis that sustained mild hypercapnic breathing, itself, could potentiate the development of hypertension in sodium-loaded individuals via activation of a cell membrane sodium-hydrogen exchanger, expansion of plasma volume and stimulation of circulating sodium pump inhibiting compounds.